The synaptic organization of monoaminergic and peptidergic fibers in the lateral horn of the rat spinal cord was studied under electron microscopy by immunocytochemistry ABC method. TH, 5-HT, SP and L-ENK immunoreactive fibers in the lateral horn were unmyelinated. In the cell clusters of the lateral horn these fibers appeared in the space between cell bodies and some pressed on the soma, but axosomatic synapses were seldom found. Many immunoreactive fibers ran along the dendrites, especially in the dendritic bundle. Occasionally a small bundle of unmyelinated fibers all contained the same kind of substance. Majority of the immunoreactive boutons formed axodendritic synapses. All the four kinds of neuroactive substancecontaining boutons or varicosities contained almost round clear vesicles or plus a few large granular vesicles. The SP and L-ENK varicosities included more large granular vesicles than the boutons did. Both symmetrical and asymmetical contacts were encountered in TH, 5-HT, SP and L-ENK boutons.

The ultrastructural characteristics of the lateral horn of the cat and rat revea-led by present study included:(1)The neurons of cell clusters in the lateral hornwere fusiform or oval,oriented rostrocaudally and possessed similar fine structures.The dendrites often protruded from the rostral and caudal poles of the cell bodies.The synapses on neuronal somata were sparse,for usually only 0-5 buttons contac-ted the plasmalemma in each neuronal profile.A little amount of neuropil existedbetween cell bodies in the cell clusters,even sometimes the plasma membranes ofadjacent cell bodies apposited directly.(2)Most dendrites in the lateral horn ranlongitudinally and paralleled with one another.Numerous dendrites aggregated inthe ventral part of the cell clusters,constituting a dendrite bundle in which adja-cent dendrites apposited directly and were surrounded by glial processes.(3)Manyunmyelinated fibers and fiber bundles ran longitudinally in the lateral horn.Theywere parallel with the neuronal and dendritic profiles.Unmyelinated fiber bundlesconsisted of the fibers with diameter less than one micron,and their terminal bottonsoften compacted together.(4)The majority of the synapses in the lateral horn wereaxodendritic synapses.A small number of axosomatic and axoaxonic synapses werefound,occasionally synaptic glomeruli and serial synapses were observed.Most ofthe buttons contained round clear vesicles and some plus a few granular vesicles.

ObjectiveTo explore the clinical feature of severe hand, foot and mouth disease (HFMD) in pediatric patients, and to observe the hemodynamic changes in those with acute pulmonary edema.Methods A prospective observation study was conducted. Thirty-five severe HFMD pediatric patients with acute pulmonary edema admitted to the intensive care unit (ICU) and Department of Pediatric of First People's Hospital of Foshan from May 2008 to September 2014 were enrolled. The clinical features were thoroughly investigated. Hemodynamic data were monitored by pulse-indicated continuous cardiac output (PiCCO) in 5 cases, and the changes in PiCCO parameters were observed at ICU admission (0 hour), and 24, 48, 96 hours after treatment.Results Thirty-five patients who met the diagnostic standard of severe HFMD were enrolled, including 22 male and 13 female, aged from 7 months to 4 years. Six patients were younger than 1 year, 13 1-2 years, 12 2-3 years, and 4 patients 3-4 years old. The most common time of occurrence of pulmonary edema was 3-4 days after the onset of the disease. Fever and central nervous system symptoms were found in all the patients, and examination of the cerebral spinal fluid (CSF) revealed non-bacterial inflammatory changes. PiCCO results showed a tendency of lowering of heart rate (HR), systemic vascular resistance index (SVRI), and extravascular lung water index (EVLWI) after the treatment, and the values obtained at 96 hours were significantly lower than those at 0 hour [HR (bpm): 119.0±14.7 vs. 200.8±19.7, SVRI (kPa·s·L-1·m-2):148.9±14.6 vs. 209.6±58.7, EVLWI (mL/kg): 10.5±1.9 vs. 34.8±10.8,P< 0.05 orP< 0.01], global end-diastolic volume index (GEDVI) was also gradually decreased without significant differences among all the time points, together with a tendency of increase in stroke volume index (SI) and cardiac index (CI). The values of the parameters at 96 hours were significantly higher than those at 0 hour [SI (mL/m2): 38.5±6.5 vs. 17.4±2.8, CI (mL·s-1·m-2): 75.0±8.0 vs. 55.5±8.5, bothP< 0.01]. Left atrium was found to be enlarged, and left ventricular systolic function decreased in two patients by cardiac ultrasonic. Four out of 35 patients died, and functional disability of extremities was found in 1 patient. Other patients were cured and discharged without any sequelae.Conclusions Severe HFMD complicated by acute pulmonary edema is a perilous condition in children, accompanied commonly by pathologic changes in central nervous system and systolic dysfunction of left ventricle. According to the results with PiCCO monitoring, HFMD patients suffering from acute pulmonary edema may be of cardiac origin in addition to neurogenic origin.

Objective:To investigate the prognosis after salvage radiotherapy with or without hormone therapy for prostate cancer.Methods:From May 2014 to December 2020, 248 patients undergoing salvage radiotherapy due to prostate-specific antigen (PSA)persistence or biochemical progression after radical prostatectomy at Sun Yat-sen University Cancer Center (n=157) and West China Hospital, Sichuan University (n=91) were analyzed. Median age was 66 (45-78) years old. Median PSA was 23.50 (0.18-845.00) ng/ml. The number of PSA persistence and biochemical progression were 143 (59%) and 105 (42%). The number of pT 2, pT 3a, pT 3b, pT 4, and unknown T stage was 99, 49, 78, 15 and 7 cases.The number of N 0, N 1 and unknown N stage was 153, 44 and 51 cases. 165 cases had positive surgical margin. Gleason score of 6, 7, 8, >8 score and unknown was in 12, 104, 34, 90 and 8 patients. Early and late salvage radiotherapy was performed in 117 and 131 patients, and 70 patients (28%) were CRPC. Hormone therapy was used combined with radiotherapy in 182 patients (73%). PSA decline after radiotherapy was compared with Chi-squre test. Kaplan-Meier method and log-rank test were used to compare progression free-survival (PFS)after radiotherapy. Univariate and multivariate analyses of PFS were performed using Cox proportional hazards model. Early salvage radiotherapy was defined as PSA≤0.5 ng/ml before radiotherapy, and late salvage radiotherapy was defined as PSA>0.5ng/ml. Results:PSA response (PSA decline ≥50%) rate was 94% (233/248), and 82% (203/248) patients had PSA decline ≥ 90%. Twelve (5%) patients had rising PSA after completing radiotherapy, but only 4 (2%) had real progression. The median PFS was 69 months (95% CI 68-70), and 3-year and 5-year PFS rate were 80% and 67%. PFS of PSA persistence and biochemical progression were similar ( HR =0.71, 95% CI 0.37-1.37, P=0.311). Compared with late salvage radiotherapy, early salvage radiotherapy had better PFS [69 (95% CI 68-70) vs. 59 (95% CI 44-74) months, P<0.001]. Compared with hormone sensitive, castration-resistant was associated with worse PFS (5-year PFS rate 74% vs. 51%, P<0.001). In multivariate analysis, Gleason score>8, castration-resistant and late salvage radiotherapy were unfavorable prognostic factors. Conclusions:In patients receiving salvage radiotherapy with or without hormone therapy for PSA persistence and biochemical progression after radical prostatectomy, high PSA level before radiotherapy and castration resistant is associated with poor prognosis.

Objective: To explore the relationship between serum complement 1q (C1q) and C1q/tumor necrosis factor-related protein 1 (CTRP1) levels in patients with coronary atherosclerotic heart disease (CHD) and their clinical value. Methods: Case-control study.115 patients with CHD who were hospitalized in the Department of Cardiology of Ningxia Medical University General Hospital from January 2018 to November 2018 were selected as the case group, including 72 males and 43 females, aged 35-82 years, average (59.96±9.49) years old. There were three subgroups: stable angina group (SAP, n=12), unstable angina group (UA, n=69), and acute myocardial infarction group (AMI, n=34). The control group was selected from 43 healthy subjects in the same period, including 21 males and 22 females, aged 23-71 years, with an average of (45.00±10.66) years old. Serum C1q and CTRP1 levels were tested by immunoturbidimetry and ELISA, and other biochemical indicators such as triglyceride (TG) and total cholesterol (CHOL) were detected.Multiple linear regression was used to analyze the influence of various factors on C1q level. ROC curve and area under the curve (AUC) to explore the diagnostic value of C1q and CTRP1. Results: The C1q level in the CHD group (184.06±31.05) mg/L was higher than that in the control group (122.22±28.18) mg/L (t=-11.405, P<0.001). The AMI group (192.80±34.08) mg/L was significantly higher than the SAP group (169.17±27.13) mg/L (t=-2.328, P=0.021).The CTRP1 level in the CHD group [241.85(79.38)] ng/ml was lower than that in healthy control group [292.7(67.64)] ng/ml (Z=-3.64, P<0.001). Group B with higher Gensini score (t=3.672, P<0.001) and group C (t=2.529, P=0.013) had higher C1q levels than group A.After adjusting for the effects of age, sex and other indicators, C1q levels were correlated with HDL-C (β=-0.582, P<0.001),CHOL (β=0.384,P<0.001) and systolic blood pressure (β=0.142,P=0.038). The ROC curve shows that when the CHD is diagnosed, the sensitivity of C1q level >150.82 mg/L is 87%,the specificity is 88.4%, and the AUC is 0.942. The corresponding sensitivity and specificity of CTRP1 <281.80 ng/ml are 76.5% and 60.5% respectively, and the AUC is 0.688. The AUC obtained by combined predictors was 0.944, and the sensitivity and specificity were 89.6% and 86.0% respectively. When AMI is diagnosed, C1q level >178.3 mg/L, corresponding sensitivity and specificity are 70.6% and 66.1%, the AUC is 0.726, CTRP1 has no diagnostic value. Conclusions Serum C1q levels in patients with CHD are elevated, and AMI patients are higher than SAP patients; C1q may be a potential marker reflecting the severity of coronary artery disease; there is no significant correlation between serum C1q and CTRP1 in CHD patients.